Jaquet Delphine, Leger Juliane, Czernichow Paul, Levy-Marchal Claire
INSERM Unité 457, Hôpital Robert Debré, Paris 75019, France.
Curr Diab Rep. 2002 Feb;2(1):77-82. doi: 10.1007/s11892-002-0062-x.
The metabolic and cardiovascular complications associated with in-utero undernutrition have been identified during the past 10 years. Reduced fetal growth is independently associated with an increased risk for the development of cardiovascular diseases, the insulin resistance syndrome and its components: hypertension, dyslipidemia, impaired glucose tolerance, and type 2 diabetes. All appear to result from the initial development of insulin resistance that seems to be a key component underlying this association. Several hypotheses have been proposed over the past 10 years to understand this unexpected association. Each of them points to either a detrimental fetal environment or genetic susceptibilities or interactions between these two components as playing a critical role in this context. The hypothesis that this association could be the consequence of genetic/environmental interactions remains at the moment the most attractive. Although the mechanism remains unclear, there is also some evidence that adipose tissue plays a role in the emergence of insulin resistance associated with in-utero undernutrition.
在过去十年中，与子宫内营养不良相关的代谢和心血管并发症已被发现。胎儿生长受限与心血管疾病、胰岛素抵抗综合征及其组成部分（高血压、血脂异常、糖耐量受损和2型糖尿病）的发生风险增加独立相关。所有这些似乎都源于胰岛素抵抗的最初发展，而胰岛素抵抗似乎是这种关联背后的关键因素。在过去十年中，人们提出了几种假说以理解这种意外的关联。每一种假说都指出，有害的胎儿环境或遗传易感性，或这两个因素之间的相互作用在这种情况下起着关键作用。这种关联可能是遗传/环境相互作用的结果这一假说目前仍然最具吸引力。尽管其机制尚不清楚，但也有一些证据表明，脂肪组织在与子宫内营养不良相关的胰岛素抵抗的出现中起作用。
